Orthopaedics Mbchb4

ANKLE FRACTURES

Anatomy
The tibio-talar articulation is not flat – rather it has two shallow condylar projections from the talus w matching depressions in the tibial plafond
Fibula – carries approx 10% of axial load

Ankle #s
One of the most common #s in adults
Severity of original insult correlates directly w the extent of articular surf damage and is an impt prognostic feat

Classification
By location +/or mechanism
AO system – Location - Type A (medial malleolus), Type B (lateral malleolus), Type C (Above syndesmosis) - (60% interobserver agreement)
Lauge-hansen system – mechanism of injury (Stages 1-6) - (50% interobserver agreement)
Determine degree of comminution (>2 fragments) of any # (esp at joint surface) and whether # open or closed
Note – if an ankle injury has occurred w displacement at the joint surf → there is likely to be a # of the fibula
This can occur above the syndesmosis + may be as high as the prox neck of fibula (get XR whole bone if nothing seen on initial ankle XR)

Clinical Examination
Hx Clear hx of a sig event – pt unable to weight bear afterwards
Rapid onset swelling (med and lat) – due to the ankle heamarthrosis that occurs
O/E 1. Gross deformity
2. Ankle instability
3. Crepitus
4. Localised bony tenderness – use ankle Ottawa rules as a guide to where bony tenderness can be elicited
Note It is impt to feel for tenderness over the medial ankle ligament as injury here has impt implications on ankle biomechanics and congruency
Displaced lateral malleolar #s do not result in altered joint contact area provided the medial structures are intact
Disruption of the medial lig leads to significantly diminished contact area

Ixs
Suspect # → Plain XR – AP, Lateral, Mortise (add longer film of entire leg if suspect prox fib #)
Key issue – determine whether ankle joint is congruously reduced → incongruency requires surg intervention provided pts gen cond + soft tis allows it

Mgt
Attempt to correct any obvious ankle deformity – early splintage will help maintain any reduction achieve
This minimises soft tis injury + swelling allowing safer + earlier intervention
Padded plaster of paris back slab → ideal method of early stabilisation

Simple (aka closed) # + joint well reduced + no evidence of medial lig injury
Good result from conservative tx with a cast
If these conditions met - pt allowed to weight bear at 2 wks provided they are comfortable
Crutches 6 wks
Use of a removable ankle immobiliser from 3 wks may make it easier for pt (if compliant and reliable)

Displaced # + joint surf has at some time been incongruous
Internal fixation of the #
Disruption of the medial lig often a clin dx but if this suspected, clinician should have low threshold for recommending surg tx
Plan any surgery for when pts soft tis and gen med cond are adequately dealt w

  1. fixation in elderly can be fraught – more conservative approach sensible provided ankle joint can be maintained in a reduced position

Open (aka compound) #s
Deal with expeditiously – goals of tx are –
Take cultures early to identify potential pathogens
Initiate AB cover early (usu begin w cephalosporin)
Plan for imeed (within 6 hrs) debridement contaminated tis and thorough irrigation of the open injury (preferably in OR)
Debridement = excision of devitalised tis + foreign material from a wound
If joint open → this part of the injury must be closed – otherwise leave all open wounds open and revisit them for closure at 48 hrs

Try and definitively fix any #s initially as long as above guidelines can be satisfied and soft tissues are in appropr condition – otherwise use some form of provisional splintage until #s can be safely, definitively fixed

Goals of surgical fixation for ankle #s
Get the # anatomically reduced (returned to normal anatomy) and the joint perfectly reduced and congruent

ANKLE SPRAINS

Definitions
Sprain Soft tis joint injury to supporting structure(s) – usu involving a discrete struct such as ligament +/or capsule

  1. Bony injury involving disruption of cortical surface and usu disruption of two cortices

Ankle jnt A synovial joint of the hinge (ginglymus) type formed between the box-like mortis of distal tibia/fibula and tenon of the talus

Anatomy
Simple hinge joint with little/no translaition/rotation
Transverse tibio-fibular lig posteriorly
Tenon formed by trochlea of talus which is convex back to front and concave on sides (also broader at front)
Medial and lat ligs give additional stability/support to ankle

Medial Deltoid Ligament
Triangular originating from tip of medial malleolus (made of 4 diff ligs but these are really inseparable)
Anterior – 1. anterior tibio-talar lig and 2. tibio-navicular ligs
Middle – 3. tibio-calcaneal lig – descends vertically
Most posterior – 4. posterior tibio-talar lig

Lateral Collateral Ligament
Three separate and more distinct bands – less robust
1. Anterior talo-fibular lig - horizontal
2. Calcaneo-fibular lig – vertical
3. Posterior talo-fibular lig – horizontal

Ankle Sprains

Most common ligamentous injury and almost always involve damage to the lateral ligamentous structures
Ant talo-fibular lig – most vuln lig in inversion and plantarflex (most common position for ankle sprains)
More severe injuries involve calcaneo-fibular lig (more vulnerable when ankle in dorsiflex)

Classification Lateral Ankle sprains classified by severity (graded 1-3)
Grade 1 – mild stretching of fibers within lig – no evidence of laxity
Grade 2 - partial tear of ant talo-fib lig and calc-fib ligs w mild laxity but good overall stability
Grade 3 – complete ruptures of ATF and CF ligs and cause potentially unstable joint (↑ swelling but oft ↓ pain due to n damage)

Clinical Examination
Hx Rolling or going over ankle (may be a past hx of similar injuries)
O/E Palpation over lateral ligamentous complex should elicit specific tenderness at site of ligament(s) involved
Swelling both med and lat due to ankle hem-arthrosis that occurs w severe injuries
As injury becomes less acute, oft possible to test for lig instability by taking ankle into inversion + comparing to uninjured side
Talar tilt/stress test – calcano-fibular lig
Ant glide/drawer test – ant talo-fib lig (pull foot forward while stabilising tibio-fib part of ankle)

Ixs Plain XR – if # suspected or if ankle takes longer to settle than anticipated (may indicate injury to articular surf talus “talar dome #”)

Ottawa Ankle Rules*
Useful for deciding if XR reqd (clin studies – 100% sens for # but only 50-60% specific)
Ankle ankle rules positive and XR reqd if –
1. Bony tenderness post edge or tip of lateral malleolus (6cm)
2. Bony tenderness at post edge or tip of medial malleolus (6cm)
3. Base of 5th Metatarsal
4. Navicular bone
5. Inability to bear weight both immed after injury AND during examination (4 steps regardless of limping)
If there is no tenderness A→D and pt can weight bear → It is NOT a #

Mgt Acute Lateral Sprains
Surgery is rarely recommended for the tx of ankle sprains
RICE – initially
Crutches may occasionally be reqd
Crepe bandage or pull on sleeve support – will make the pt more comfortable
More swollen and severe sprains – can be immobilised in a cast or splint 4 wks to allow acute sxs to settle
Once acute sxs begin to resolve → rehab (peroneal strengthening, range of motion exercises and proprioceptive retraining) – joint function + prevention
Proprioceptive training – eyes closed, one foot, balance
Delay return to sport until rehab well on the way – return with bandage/sleeve

Mgt Chr Lateral Instability
Surgery – last resort (many diff procedures available)
Indications for surgery – crippling instability preventing adequate level of function for individual pt after adequate rehab attempted
Requires >3 months supervised proprioceptive retraining and peroneal strengthening
Stress XRs prior to recommending surgery to confirm degree of instability + provide evidence to support an op for your pt
After a period of immobilisation post-op – pt undergoes further intensive period of rehab

BACK PAIN


Objectives 1. Appreciate the spectrum of back pain
2. Red flags and Yellow flags
3. Sciatica and what causes it
4. Dx a lumbar disc herniation
5. Know when to refer a pt w – lower back pain + lumbar disc herniation for a specialist opinion
6. Appreciate the limited need for surgical tx for the adult pt w low back pain
7. Awareness of high incidence of organic path in children who have back pain

Etiology of LBP (low back pain)
Assoc w work-related lifting and forceful mvments
Assoc w exposure to whole body vibration
Assoc w heavy physical work and work related awkward postures

Hx
Most back injuries see to be the result of accumulated small injuries or back stress rather than one specific injurious episode (back fatigue)
You can not deal w back pain in isolation from the pt – explore fear of ca, pain compensation, work requirements etc
Look out for red flags
Differentials – Trauma (can be minor if assoc age + osteoporosis)
Inf – uncommon infections eg TB, Brucellosis
Inflam – AS, RA, OA
Neoplastic – 2ndry tumors
Congenital – lumbar/sacral variations, hemivertebra, spina bifida, other deformities
Others – strains/sprains
Refered back pain –
Abdominal organs – pancreas, kidney, pelvic viscera
Vascular – AAA
Systemic illness – back pain a freq sx
Specific questions to ask –
Presence of gen sxs
Gradation of pain + fluctuations w activity → functional limitations
Night or supine pain → suggestive of malignancy or infective process
Morning stiffness → inflam dis
Radiation of pain, pins + needles, numbness, strength → neuro impairment
Competency of sphincters, presence of saddle anaesthesia → cord embarresment
Changes on hills or stairs → claudication, spinal stenosis

RED FLAGS

Patient <20 or >50*
Injury Significant trauma* (can be minor in older pt w osteoporosis)
Pain feats Progressive pain
Continuous pain
Severe unremitting night time pain*
Pain that gets worse when pt recumbent*
Alternating or bilateral sciatica
Spine movements painful in all directions
PHx Cancer*
IV drug abuse*
Systemic steroids*
HIV
O/E Localised bony tenderness
Pain or tenderness thoracic spine
Systemic sxs – weight loss*, night sweats, fever*, lethargy
Neurological sxs - Weak legs
CNS deficit at more than one root level
Bilateral signs of nerve root tension
Cauda Equina Syndr* - Saddle anaesthesia / Recent onset bladder dysfunction / severe progressive neurological deficit

YELLOW FLAGS (Psychosocial Concerns – not predictors of occurrence but are predictors of successful rehab)

Attitudes and beliefs about back pain – eg a pt who believes they will be disabled is more likely to become disabled
Behaviours
Compensation issues
Dx and Tx issues
Emotions – eg fear avoidance – people fear there is something wrong with their back
Family
Work

Examination Sore Back
Patient to remove clothes
Examine full ROM – flexion, ext, lateral flex, rotation (back and neck)
Examine SLR, sacro-iliac joints, hip joints

Mgt Sore Back
Most backs get better by themselves
Bed Rest – inappropriate except in the most severe cases (should not exceed 2 days)
Activity improves func and allows greater numbers of sore backs to resolve → water exercises are esp beneficial (eg swimming)
Pain does not (usu) signify further damage
Every employer has easy jobs that need doing
Education safe lifting practices – prevent further occurrences

Time from onset Assessment Action
0-4 weeks No red flags, normal neuro exam Reassurance, education, normal activities, Rx paracetamol/nsaid
4-6 weeks Full reassessment – no red flags/normal neuro Plain XR, ESR, treat as above, trial of manipulation/other therapies
Refer for opinion and imaging

Stay at work

Non-surgical Mgt Back Pain
Therapy Adv Disadv
NSAIDs Effective 1st month Side effects
Physiotherapy Keeps pt busy Ineffective
Manipulation Effective 1st month Potential for trauma
Acupuncture/TENS Provides temporary relief Inffective LT
Exercise Proven effect Can cause ↑ discomfort
TENS = transcutaneous n stimulation (method of pain relief)

Medical Mgt of Acute Lower Back
Improved outcome Early NSAIDs
Return to work and maintained mobility
Exercise program and aerobic fitness
Restorative sleep
Worsened outcome Poor work satisfaction
Previous chr pain (+ migraines, IBS, CFS (chr fatigue syndr), Raynaud’s phenomenon)
Severe sleep disturbance +/or depr
Compensation
Bed rest (>48 hrs)
Illness beliefs

SURGICAL ASPECTS OF LBP

Pathological causes of Back pain
Congential Sciolosis
Infection discitis, osteomyelitis, TB
Trauma #s and # dislocations assoc w a hx of sig trauma (path # may occur if a v low energy injury occurs)
Neoplasia Mets, Primary bone tumor spine rare, Other neoplastic processes incl multiple myeloma, lymphoma
Metabolic #, pain or deformity from osteoporosis, osteomalacia, hyperparathyroidism
Degenerative
Inflammatory AS, Seronegative spondylo-arthroapthy

Scoliosis
Lateral curvature of spine w rib rotation (deformities persist when pt bends forward)
All cases – refer for specialist assessment
Minor scoliosis noted on a radiological report w/o evidence of clinical deformity seldom requires intervention when an isolated finding

Infection
Pres Severe back pain not relieved by rest, fever, systemically unwell
O/E Tender spine w loss of motion
Ixs ↑ ESR, ↑ wcc, blood cultures may be positive, bonescan hot in region of inf
Radiological changes – later devt of loss of disc space, end plate irregularity adjacent to disc, possible paravetrebral abscesses
Direct biopsy – determines whether inf pyogenic, TB or brucellosis (rare)

Tumor/Neoplasia
Most common – mets (breast, prostate, thyroid, lung, kidney, gut, melanoma)
Pres Severe back pain w hx of weight loss, pain not relieved by rest
O/E Loss of motion possible
Ixs Destructive lesions of bone incl loss of the pedicle on AP, disc often preserved, bonescans generally hot (but may not be in myeloma)

CAUDA EQUINA SYNDROME
Def Compression of the whole cauda equine within the lumbar spine → damage to sacral nerve roots
Etiology Eg. massive central disc hernation
Pres Saddle anaesthesia (genital/perianal sensation)
Sphincter dysfunction – lack of control of bladder and bowel function
Sudden onset neurogenic incontinence (not stress or urge incontinence) is an EMERGENCY
Prognosis W/o tx – Effects of permanent damage are disabling

SCIATICA*
Def Pain radiating down the lower limb along the path of the sciatic n and either of its two divisions (posterior tibial or peroneal nerves)
Implies involvement of the lumbar nerve roots (commonest origin)
Distbn of pain relates to the level of the involved n roots
Pres Pain described as sharp
May have assoc sensory sxs – tingling, numbness, dysaesthesia
Motor weakness may occur + reflex changes reflecting n root involvement
Low back pain (if present) is the lesser complaint compared w the sciatica

RADIATING LEG PAIN
Occurs in the buttock and post thigh and comes from the low back
It is often misdx as sciatica
It is seldom below the knees (but is possible)
Normally when present w back pain, the radiating leg pain is the lesser of the 2 sxs

NEUROGENIC CLAUDICATION
Due to compression of the cauda equine 2ndry to spinal stenosis
Pain in the legs freq within dermatome or distbn and sometimes assoc w neuro sxs
Precipitated by walking + may occur w prolonged standing
Classically relieved by sitting or flexing the lumbar spine
Differs from vascular claudication in the distbn of pain and method of relief
Pts w claudication 2ndry to PVD → normally get relief by standing w/o the need to flex or sit

DEGENERATIVE LUMBAR DISEASE
Aging → degen lumbar spine
Disc nucleus desiccates + annular fissures develop → bulging of disc wall
Height of disc + overall spine ↓
↑ facet joint load → devt of OA
Rship betw path and back pain variable
Bulging discs + facet osteophyts can narrow the n root canal → n root compression w sciatica or neurogenic claudication

DISC PROLAPSE*
Localised annular fissures allow bulging or failure of the disc w prolapse of nucleus/cartilage end plate/nuclear material
Usu post-lat direction into spinal canal → may cause compression + nuclear contents may inflame the n root → sciatica + potential neurological disturbance
Anat Most common – L5 + S1 (90%) - Occasionally L4
L4-L5 Disc → L5 Root → EHL ↓ power / ↓ sensation L5 dermatome / normal reflexes
L5-S1 Disc → S1 nerve root → weakness on plantarflex possible / ↓ sensation S1 dermatome / ↓ ankle reflex
Central massive disc protrusion → cauda equina syndr
Pres Lumbar Disc Hernation
Pt usu young (20-50) + active
Traumatic incident usu – bending, lifting or twisting (can be minor) → v sore back + pt may be unable to get out of bed the next morning
Pain moves to sciatic distbn
Pain ↑ w cough or sneeze
Paraesthesia (numbness + weakness) possible
Look for bladder or bowel sxs (cauda equina syndr)
O/E Signs of n root irritation – backward stance, ↓ SLR, crossed SLR, lassague, bowstring
Sings of altered n root conduction – motor, sensory, reflex, sphincter
Local back signs
General – abdo, rectal etc
GP Mgt Establish a working dx
Ixs - Hb, WCC, ESR
Temp
Is pt sick?
Think carefully before making this dx in older pts, anyone w fever, anyone w known malignancy
No XRs unless indicated
Natural hx is resolution of acute episode within 1-6 wks – some recur periodically throughout life
Exclude cauda equina syndr (exclude neurological signs)
Vast majority can be managed at home + expect gradual recovery over 3-4 wks
Bed rest if only absoulutely necessary (<2 days) – firm mattress, any position
Pain relief
Sedation
Epidural steroid
Indications for referral of Lumbar disc herniation*
Severe motor or sensory loss (initially)
Signs on adequate conservative tx
Failure to settle within 4-6 wks
Signs of paraplegia
Belated signs and sxs
Sphincter disturbance → IMMEDIATE REFERAL
Ixs XR lumbar spine to rule out bony lesions, CT, MRI
Surgery Laminectomy, Discectomy, Fenestration, Spinal fusion

SPINAL STENOSIS
Pres Older pt, past hx back pain, usu gradual onset
Neurogenic claudication or sciatic pain bilateral + equal
O/E Preserved lumbar flex but loss of lumbar ext
May have normal neurology + normal SLR
May be abnormalities assoc w any n root involvement
Periph pulses normal
Hip ROM normal and pain free
GP Mgt Analgesia
Ixs – XR (ageing changes, spondylolisthesis or scoliosis), may require CT/MRI
Tx Surgical – decompression (removal of pres) + fusion (only if pre-existing or operative destabilisation of the spine)

SPONDYLOLYSIS
A pars interarticularis defect (segment of bone betw sup and inf articular facets esp of lumbar spine)
Defect is 2ndry to stress # or injury
May cause variable sxs incl pain or sciatica involving the n root exiting under the pars interarticularis (eg L5 spondylosis involves L5 root)
Slippage betw the vertebral bodies may occur resulting in Isthmic Spondylolisthesis

BIOLOGY OF PAIN


Exam – long answer question

Pain
Unpleasant sensory and emotional experience assoc w actual or potential tis damage
Pain perception does not correlate w the degree of tis damage
Pain is subjective – each pts experience and expression of pain is diff

Pain Classification
Two main types of Pain –
1. Nociceptive – due to direct stim of periphe nerve endings (eg wounds, #s, burns, angina)
2. Neuropathic – due to dysfunction of pain perception sys within periph or centr nervous systems due to injury, dis or surg damage (eg phantom limb pain)

Alternative Classification of Pain
1. Physiological pain
a. Nociceptive pain - somatic and visceral pain (predom due to input to the sp cord and brainstem)
b. Non-nociceptive pain – predom due to SNS pain Pathophysiology w or w/o afferent input to the sp cord and brainstem (eg. Chronic pain syndr – CPS)
c. Mixed nociceptive and non-nociceptive pain
2. Psychological pain
a. Somatoform disorders – somatisation d/o, conversion d/o, pain d/o, hypochondriasis, body dysmorphic d/o, undifferentiated
genuine dis but no physiological basis (the more sxs a pt presents w, the more likely it is to be psychosomatic)
b. Factiitious d/o (eg inventing pain to get a benefit or love from family etc)
c. Malingering
d. Others
3. Mixed physiological and psychological pain

Physiology of Pain
A and c fibres – transmit from nociceptors to dorsal horn
Dorsal horn of spinal cord – 2nd order neuron of spinothalamic tract is subject to modulation by a number of influences in addition to its synapse w nociceptor fibres
Large mechanoreceptor fibers destined for the dorsal column also synapse w 2nd order spinothalamic neurons and with interneurons of the grey matter of dorsal horn
Nociceptor neurons release NTs (eg Substance P) in addition to excitatory transmitters → influence excitability of spinothalamic neurons
Neurons in the dorsal hron also subject oto modulation by desc fibers from the peri-aqueductal grey matter of the midbrain and raphe nuceei of the medulla
These neurons are activated by endogenous opiate (endorphin) peptides
Dorsal horn – is far more than a waystation → it gates and modulates info about painful stimuli before it ascends in the spinothalamic tract
Dorsal horn = integration + transmission
The perception of pain is further influenced in the diencephalon by rich interconnections of the thalamus to the limbic sys
Hypersensitivity – LT potentiation via repeated depol of glycine/glutamate NMDA Ca/Na channels and wind up due to Mg2+ plug expansion

Components of Pain
Total pain is due to interaction of social, psychological and biological factors → perception of pain
Social factors – loss of job/income, role in family, social position, friends, independence
Psychological factors – fear (pain, hospital, future, dying), anger (dx delay, therapeutic failure, unavailable doctors, bureaucratic bungles), depr
Factors such as emo distress, coping skills, work satisfaction and illness beliefs → adversely affect func and recovery (ie exaggerate and prolong disability)

Pain Mgt
Mild pain → 1g paracetamol
Moderate pain → 1g paracetamol + 30mg codeine (or 400 mg ibuprofen)
Severe pain → 1g paracetamol + 30mg codeine + 400mg Ibuprofen

WHO Analgesic Ladder
Start Non-opioid analgesic eg Paracetamol, NSAIDs
Add Weak opioid eg Codeine, Dihydrocodeine
Substitute Weak opioid replaced by strong opioid eg Morphine (immediate release)

Opioid Side Effects Mgt
Constipation Regular laxative
Dry mouth Freq sips water, sugar free gum
N/V Anti-emetic
Sedation Explanation, avoid other sedating meds

Feats of Neuropathic Pain
Burning, stabbing or pulsing pain
Spontaneous pain, w/o ongoing tis dam
Pain in an area of sensory loss
Presence of a major neurological deficit (eg sp cord trauma)
Pain in response to non-painful stimuli (allodynia)
↑ pain in response to painful stimuli (hyperalgesia)
Unpleasant abnormal sensations (dysaesthesias)
Poor relief w opioids alone

Mgt of Neuropathic Pain
Anticonvulsants – eg gabapentin, pregabalin
Antidepressants – eg amitriptyline
Ketamine

Clinical assessment and mgt of chronic pain
1. Nociceptive element
2. Non-nociceptive physiological element – past or fam hx of pain, neuroendocrine conditions (DM, thyroid), co-morbidities (eg migraine), neuro signs
3. psychological element – past or fam hx of mental health probs, devtal hx
4. consequential problems – impaired sleep, chr fatigue, depr disuse atrophy

Mgt of Chronic (non-cancer) pain
1. Psychological mgt – CBT, exercise based mobilisation, mgt of illness beliefs, tx of depr and other psychological conditions
2. Physiological mgt – sleep restoration and analgesia – antidepressants, anticonvulsants, hormone replacement, NSAIDs, Opiates, acupuncture, fitness NNT for analgesics to achieve 50% relief (amitriptyline 2.8, gabapentin 5, codeine 18)
3. Vocational (ergonomic) and psychosocial mgt – return to some meaningful social engagement
Key Message – Mgt of chronic pain is HOLISTIC – psychological, social, pharmacological etc

LOCOMOTOR – KNEE LIGAMENT AND MENISCAL INJURIES

Clinical Assessment

Hx Mechanism of injury
Pop or snap (high correlation ACL injury)
Pain (severity does not correlate w severity of injury)
Swelling (most impt indication of injury severity)
Instability
Hx prev injury

O/E Swelling
Focal tendernss
Ligament laxity – Collaterals, Cruciate (lachman test)

Swelling Hemarthrosis - <1 hr onset, painful → torn ACL until proven otherwise
Patellar disloc – 2nd most common cause
Effusion – normal looking synovial fluid, delayed (overnight), uncomfortable → minor sprain or meniscus

Ixs XR – plain or stress
Aspiration – lipohemarthrosis = #
MRI
Arthroscopy

Collateral Ligament Injuries - Contact injuries – external forces - Grade 1-3

ACL Most common knee lig injury in sport
Non-contact wrenching injury
Feats - Hear pop or snap, pain (unable to continue), hemarthrosis

PCL Less common – typically dashboard mechanism w direct blow to prox tibia while knee flexed
Pain chief complaint, instability less so, LT joint degen may be inevitable

Chr Ligament Instability
Muscle rehab impt first line tx
Knee braces – helpful in sport
Ligament reconstruction

Meniscal Problems
Anatomy 2 menisci – lat and med
Semi-lunar shaped sitting betw tibia and femur
Fibrocartilage (collagen fibers circumferential)
Function – share load bearing w the articular cartilage
Damage → ↑ contact stress betw articular surfaces → predis to joint degen (↑ wear and tear on remaining articular surface)
Tear in the avascular zone (central 2/3) unlikely to heal – tears in the vascular zone may heal and sometimes suitable for repair
Meniscal Pathologies
Congen Discoid not semi-lunar menisci (often asx but susceptible to tearing)
Hypermobile meniscus – displacement in and out (sxs of catching and locking)
Acqd younger pts (assoc w lig injuries and hypermobility) cf older pts (degen tears of menisci)

Dx Hx and phys exam – sufficient in many cases but if unclear, use MRI
Hx Mech injury – acute injuries → twisting or pivoting action
Swelling – generally over several days (rapid swelling → ligament injury or patellar disloc)
Tenderness – joint line
Pain and catching – pivoting or rotating movements (generally not when movement in straight line)
Locking – only if sig meniscal fragment displaced into joint (pts describe eg squatting (knees flexed) + feeling sthing move + cant straighten
Sensation of knee unlocking – pts describe sthing moving and then moving freely again (classical for unstable meniscal tear)
Congen abnormalities (often bilat) – pts describe painless clunking and mechanical sxs over long period then painful when meniscus torn
O/E Effusion often present with meniscal tear
Localised tenderness over affected meniscus and rotational stressing of flexed knee provokes pain (meniscal grinding test)
Localised swelling over meniscus → meniscal cyst
When assessing meniscal tear → exclude an assoc ligament injury (test all ligs) and exclude patellar instability and identify signs of patellofemoral pain
Ixs Plain XR – does not dx meniscal path (but help exclude other conditions esp weight bearing AP XR to determine pre-existing joint degen dis)
MRI
Tx Arthroscopic tx – surgery through small stab incisions
Degen tears and flap tears – resection unstable fragment
Longitudinal tears – sutures or absorbable arrows → stable menisci back together
Discoid menisci – resect abnormal portion and torn portions leaving as much of normal rim as possible
Symptomatic hypermobile menisci – suturing menisci down to periph capsule to stabilise
Meniscal cysts – removal inf leaf of horizontal cleavage tear → decompresses valve effect + allowing cysts to decompress itself

MUSCULOSKELETAL RADIOLOGY

Use plain film; MRI/bone scan only used if suspected or occult fractures

What plain film features indicate a # is present
• black line across bone (respresents a break or separation of trabeculae) – radiolucent line
• a step off in bone contour or margin (cortex irregularity)
• white line across bone trabeculae indicates compression or overlap of trabeculae (↑ bone density)
• angulation of bone segments

Indirect evidence of a fracture
• soft tis swelling
• obliterated fascial planes
• joint effusion or lipohaemarthrosis (intra-articular fracture → fat and blood leakage into joint)

What plain film clues suggest an open fracture?
• Soft tis deformity
• Bone protruding beyond soft tissues
• Intra-articular or subcut gas (surgical emphysema)
• Foreign body in soft tissues

Fracture Description
• Open or Closed (open = compound # = skin perforated + open wound down to # site)
• Complete or Incomplete
• Location
o fractures involving the shaft of a long bone are localised by dividing the bone into 1/3s
o #s at the end of bones are usu described anatomically
o Eg. femur - fracture of the greater trochanter, neck of femur fracture, intercondylar #
o Eg. elbow – supracondylar fracture
o Eg. ankle – medal malleolus fracture
• Type
• Displacement
o Occurs when ends of the bone have shifted relative to one another
o Described by the relative position of the distal fragment compared to the proximal fragment
o Degree of displacement described in % terms (relative to width of bone)
o If displacement is >100% of shaft diameter, describe length of overlap or amount of distraction present
o Displacement is lateral/medial or ant/post
• Angulation
o Varus (distal fragment points medially)
o Valgus (lateral angulation where distal fragment points laterally)
o Angulation tends to be more sig than displacement
o Alteration in the plane of mvment of the joints in the lower limb results in abnormal stress on the joints and devt of post traumatic osteoarthritis
• Rotatation
o Twisting of one of the fracture fragments relative to another
o You need to see both ends of the bone to assess for rotation
o Describe in terms of degrees either laterally or medially
• Communition – 2 or more fragments; mild/moderate/severe

Incomplete #
Fracture in which the line of fracture does not completely traverse the bone
Occurs mainly in children
• Buckle # - focal compression of cortex
• Torus # - circumferential type of buckle #
• Greenstick # - periosteum and cortex fractured on one side and buckled on other
• Plastic bowing deformity – bending w/o a discrete # line

Biomechanics
Four types of loading or application of an abnormal force to a long bone
• Tension or traction – pulling apart of trabeculae often causes soft tis injury rather than #
• Compression – pressing together of trabeculae
• Torsion or rotation
• Bending

Fracture Configuration
• Transverse
o Usu caused by bending, often due to direct blow
o S/times due to traction forces at site of a tendon or ligament insertion (avulsion # - tearing away or forceful separation)
o Seen in pathological #s
o Tend to be more stable but area of bone contact small so may take longer to get stable union
• Oblique
o # at angle <90’ to long bone
o due to compression AND torsion (+/-bending)
o Higher rate of non-union than spiral #
• Spiral
o Caused by torsion or twisting
o Curve around the bone
o Large area of bone is in contact so union often rapid
o Hoever, displacement occurs more easily
• Diaphyseal impaction #
o Axial load can drive the diaphysis into the thinner bone of the metaphysis
• Comminution
o 2 or more fracture fragments
o ↑ severity of comminution usu reflects application of increasingly high energy force
o often assoc w soft tis injuries
o a butterfly fragment is a wedge shaped fragment
• Segmental
o Same bone fractured at two separate sites
o Instability and difficulty in reduction is common
• Displacement

Special Fractures

1. Growth plate injuries – Salter-harris system

Type 1 (SUFE) Type 2 (most common) Type 3 Type 4 Type 5

• Metaphysis should always line up with epiphysis
• In children, growth plate tends to # as opposed to ligaments being sprain as considerably weaker → never dx sprained lig in child!
• Tend to heal quickly (~4 wks)
• Complications of growth plate injury → growth arrest or avascular necrosis may develop (more likely with type 3/4 rather than type 2)
• This is significant bec disruption of the lines of cartilage cells that contribute to growth in length of the bone or injury to the bone supply can disrupt normal devt of bone

SUFE
• Slipped upper femoral epiphysis
• Growth plates slips into ER (adduction + extension) → ↓ IR, ↓ abduction, ↓ flexion (SUFE kid cannot flex and internally rotate)
• Common in heavy children, esp boys or Polynesian girls (10-14 y sage)
• Tx – screw across growth plate (goal is to keep growth plate from slipping, consider bilateral)

2. Pathological Fracture
• Occurs at site of a pre-existing abnormality (usu osteoporosis or a tumor)

3. Stress Fracture
• 2 types of stress # → fatigue # or insufficiency #
• Fatigue # - occurs in normal bone 2ndry to abnormal stress; repeated stress weakens the bone
o Plain films are usu normal – some time after initial sxs → cortical lucency and periosteal new bone may be present
o Eg March # common after marching, ballet or prolonged standing → 2nd metatarsal (common site of stress #)
o Bone scintography or MRI can be helpful in diagnosing a suspected fatigue #
• Insufficiency # - occurs 2ndry to normal stress on abnormal bone (usu osteoporotic)

Principles
• Always ask for at least two views
• Blood on XR – looks like muscle
• To assess rotation at a # site – difficult but can sometimes tell by comparing the diameter of the two bone segments
• Bony callus formation – appears approx after 1 month (can be 2-3 weeks in a v young person) – non-bony callus = hematoma
• Rules about suspected wrist # XR – 1. always scrutinize the scaphoid and 2. Look at the lunate (most of the serious wrist injuries)

Fracture + Dislocation Types
• SC joint disloc – uncommon; if seen on film, usu due to film misrotation
• DDH = Developmental Dysplasia of Hip (neonate’s hips easily become dislocated – due to mechanical, familial, hormonal and birth pres – F:M 9:1)
• Scapula # - v painful (muscles on scapula bounded w tight fascia → bleeding → pres against fascia → pain)
• Supracondylar # - most common elbow # in child (land on hand w elbow hyperextended) – distal humerus fragment normally displaced posteriorly
• Ulnar # - look for a radial # also or a fracture-dislocation (caused by indirect force) – unless single # of ulna due to direct force trauma
Monteggia fracture - # of prox ulna + disloc of head of radius
Galeazzi fracture - # radius shaft + disloc of distal radioulnar joint
• Acetabular # - Jagged acetabulum – will require hip replacement due to consequent OA of hip joint
• Subcapital # (NOFF = neck of femur fracture) → intracapsular hemarthrosis → risk of AVN (avascular necrosis) due to unidirectional blood supply
• Calcaneal # - LT difficulties walking on uneven ground
• Wedge compression # - generally occur in thoraco-lumbar region (unusual higher up due to thoracic spinal support via ribs)
Spinal #s most often lumbar or cervical
Ant – suggests hyperflexion injury (eg fall from height, mva)
• Scaphoid # - pain on axial loading, anatomical snuff box
scaphoid surrounded by cartilage – only blood supply via ligs (# through certain areas → vuln to AVN)
• Posterior GH joint disloc – due to violent int rotation shooting hum head backwards (electrocution, seizures)
IRs (pecs) stronger than ERs (rotator cuffs,deltoid)
• Ant GH joint disloc – when humerus abducted + externally rotated + force applied
Muscle spasms to protect joint – before reducing joint, you should try to get subscapularis etc to relax (anaesthesia is ideal)
Axillary n vulnerable – always assess deltoid sensation + gentle contr of deltoid (hold shoulder while pt tries to push back against you)
Signs – holding up arm, leaning forward + holding arm away from body
LT complication – recurrent dislocation due to ↑ laxity of joint
• Clavicle # - lifting up arm from elbow, holding arm close to body

Anatomy
• Suprapatellar Pouch – 4 fingerbreadths above sup pole of patellar → vuln to penetr injury
• Radial n – passes down the spiral groove on the post humerus (injury via # to midshaft of humerus – lies directly on bone so v vulnerable)
• Iliac crest = L4/5 intervertebral space
• Radius articulates w scaphoid + lunate (Radius-Lunate-Capitate)
• Triceps – critical muscles for getting in + out of chair (C7-8 # will cause probs)

Joints
• Sail sign (lateral elbow radiographs) – due to # of radial head (usu hemarthrosis) - suggests effusion of elbow
• Injuries that produce intra-articular hem → distension of synovium + forces fat out of the fossa → radiolucent triangular shadows ant + post to distal end of humerus (fat present within joint capsule bout outside synovium) – fat pad sign indicates presence of intra-articular hem (often assoc w intra-articular skeletal injury (usu th radial head)
• Lipohaemarthrosis – intra-articular # causing fat from bone marrow to leak w blood into joint (fat/blood layer) – aspirate blood from joint – check for fat
• Haemarthrosis – unless painful, don’t aspirate as will naturally be reabsorbed anyway
• Gas in a joint – during surgery (will get reabsorbed naturally) –
Never gas gangrene in a joint – bec clostridium anaerobe thus prefer hypoxic/ischemic areas (eg diabetic pts w PVD)

Other
• Pn.thorax – most common cause is ?perforated bulla on surf of lung
Inspect + Palpate – ↓ chest wall mvment
Percuss – Hyper-resonant
Ausu - ↓ breath sounds
• FOSH = Fall on outstretched hands
• Epiphysis – part of a long bone developed from a center of ossification distinct from that of the shaft and separated at first by a layer of cartilage
• Metaphysis – a conical section of bone betw the epiphysis and diaphysis of a long bone
• Diaphysis – shaft of a long bone
• Apophysis – outgrowth or projection, esp from a bone – a bony process or outgrowth that lacks an indep center of ossification
• Physis = growth plate
• Osteophyte – a bony outgrowth or protruberance
• Gout → bone + joint destr + swelling (esp 1st MTP joint)
• Pathological bone changes – Pagets Dis (only condition which expands bone - coarsened trabecular bone → osteosarcoma rare complic) or inf

SHOULDER INJURIES

Common shoulder problems
1. Instability – traumatic anterior dislocation and anterior sublux
2. Rotator cuff problems – impingement and rotator cuff tear
3. Acromioclavicular joint injuries

1. Instability

Traumatic anterior instability
Most common form of instability
Cause forced abduction external rotation injury (most common cause)
direct blow prox humerus pushing humeral head forward and down in glenoid
Pres Severe pain, inability to move shoulder, deformity (usu obvious)
IX XR confirms dx (AP and scapular lateral views)
Assess axillary nerve
Tx Closed reduction (shoulder gently reduced back into joint) – often requires sedation, pain relief and mus relaxation (usu GA)
Mgt High incidence recurrence (esp if ant disloc)
Surgical reconstruction to reattach avulsed capsule and ligs to ant edge of glenoid – good option for young and active
Rehab v impt following shoulder reconstruction (usu 6 months until return to sports)

Anterior Subluxation
Def Passage of humeral head anteriorly out of joint + spontaneous reduction
Pres Sensation of shoulder going out + in of joint + dead arm syndr (arm paralysed and weak for secs-mins) + spontaneous recovery of arm
O/E Mild restriction ER + positive anterior apprehension/relocation signs
Ix XR → look for evidence of minor #s
Hill-sachs lesion – glenoid rim dented into humerus
Bankart lesion – small # fragment anterior rim glenoid (capsular ligs pull away piece of bone during sublux) – tend not to heal
Mgt Rehab via muscle balance and strength

2. Rotator Cuff (RC) Problems

Anatomy RC - helps move and hold humeral head in glenoid
Subacromial bursa – separates acromion from supraspinatus tendon
Long head biceps – passes along bicepital groove of humerus – enters betw subscularis and supraspinatus – then attaches to glenoid labrum

Impingement / Tendinosus
Hx specific or repetitive shoulder injury
Pain/weakness with overhead activities
Night pain
O/E Painful arc (70-100’ abduction)
Altered scapulohumeral rhythm
Tender over gr tuberosity +/- biceps tendon
Weakness
Positive impingement sign
Subacromial LA test
Ix XR
US – assess cuff integrity (MRI usu not reqd)
Mgt Anti-inflammatory / analgesic
Mus strength and bal rehab program
Subacromial corticosteroid injection
Arthroscopic acromioplasty

2. Rotator Cuff Tear
Anatomy Supraspinatus tendon – most commonly torn component of RC (all components can be torn individually or in combo)
Hx Specific injury normal (not necessarily major trauma)
Similar pain to impingement but ↑ weakness
2ndry stiffness / frozen shoulder
O/E Altered scapulohumeral rhythm
Restricted active abduction arm but passive abduction ok
Weak RC muscles
Ix US – reliably shows any sig RC tear (MRI usu not reqd)
Mgt Sig tears w weakness - Surgical repair tendon back onto gr tuberosity (>6 month recovery)
Small tears w good function – rehab once pain settles

3. AC Joint Injury
Anatomy Normally only small amounts motion at joint (rotational)
Scapula suspended by corococlavicular ligaments
Injury falls and contact activities when person falls on to point of shoulder → pushes acromion + scapula away from clavicle
Mild sprain – ligs remain intact → marked separation of clavicle from scapula
Pres Hx + AC joint pain
If ligs disrupted → prominence outer end of clavicle
Ix AP XR shoulder → joint separation + exclude #s outer clavicle
Mgt Majority grade 1,2 or 3 → conservative mgt + sx relief
Analgesia, icing, anti-inflams, broad arm sling (elevates elbow + supports weight)
Surgical repair with more severe grades

SOFT TISSUE PROBLEMS LOWER EXTREMITIES


Soft tissues → muscles, tendons, ligaments bursae, fasia
Other soft tissues that must also be assessed in limb injury → blood vessels, nerves, skin
Muscle Strain
Tend to occur in 2-joint muscles – eg hamstrings, rectis femoris, gastroc
Tend to occur w eccentric action (muscle acts to resist lengthening)
Graded according to amount of damage
Grade 1 Few fibers injured Minimal power loss Minimal pain
Grade 2 Several fibers injured Moderate power loss Pain w contraction
Grade 3 All fibers injured Significant power loss Variable – usu severe

Muscle Contusions
Different to mus strain because –
Usu occur in deep muscles (near bone-mus interface)
Can occur anywhere in the length of the mus
Can occur in single or double joint muscles
Graded according to sxs and signs – eg. Quadriceps femoris
Grade Swelling Flexion Squat
Mild Very little >90’ Easy
Moderate Detectable 45-90’ Some pain
Severe Sig <45’ Difficult

Acute Partial Tears – eg. Tib post tendon injury
Often a longitudinal split resulting in loss of function + pain
Lengthening of tendon leads to altered foot alignment
Tx conservative (physiotherapy/orthotics) or surgical (repair/reconstruction)

Complete Tendon Rupture – eg. Achilles
Sxs Often complain of a sensation like someone kicked them in the calf
Signs Pos calf squeeze test, Palpable defect, thickening, swelling, bruising
Tx Aim to restore physiological length – conservative (equinus cast) or surgical (repair + augmentation)

Tendonitis
May be present in the early stages of tendinopathy
Sxs of inflam – morning pain + stiffness, warms up w exercise, comes back w cool-down, benefits from anti-inflammatories

Tenosynovitis
Inflammation of a synovial tendon sheath
Inflammatory
Often characterised by – Warm up and cool down, Crepitus, Swelling

Tendinopathy
Degeneration within a tendon that occurs as a result of imbalance betw overload + recovery
Tx Conservative – stretching + strengthening
Surgical - debridement

Enthesopathies
Types 1. Juvenile – growth plate overload at tendon insertions (apophysitis)
2. Adult – inflam at tendon insertions eg. Plantar fasciitis
Tx Conservative – reduce load on tendon, treat inflam, correct any underlying predisposing factors

Shin Pain
1. Periostalgia Overload condition of muscle insertions into bone presenting with –
diffuse pain along medial tibial border (usu mid/distal 1/3)
often disappears on warming up and returns on cooling down
Tx - local modalities incl massage
Correct underlying postural or biomech abnormalities
Reduce training load to allow tissues to adapt + graduated reintro of exercise
Surgery seldom reqd
2. Stress # end stge of bone overload → abnormal physiol response in bone → bone reabsorption > production → focal weakness → #
anterior tibial #s heal more slowly + ↑ likelihood of non union – due to poorer blood supply
o/e – focal tenderness + pain on hopping
ixs – plain film often normal (dx confirmed by bonescan)
tx – relative rest (may require immobilisation or non-weight bearing), education, graduated return to activity once painfree, surg rare
3. ECS (Exertional compartment syndr)
rarely progresses to surgical emergency
fascial envelopes separate grps of mus in the lower leg into 4 main c/ments – ant, deep post, sf post, peroneal
Pathophysiology unclear
Sxs – exercise causes mus tightness → pain + forces to stop exercise
May also be weakness, dysfunction, discoordination, parasthesiae
Signs - elev c/ment pressures
Swelling may cause pain by – tissue hypoxia, traction on periosteum, tension within fascia, other mediators of pain
Dx - c/ment pres testing (exercise to reproduce sxs then measure pres – immed post exercise, 2, 5 and 10 mins)
Tx - conservative measures – massage, exercise modification, orthotics (poor success rates)
Surgery defintive tx – fasciectomy/fasciotomy

Principles of Acute Soft Tissue Mgt

Aim is to ensure optimal healing evt and avoid delays in healing thereby providing a sound and quick repair

Stage 1 Injury - Cellular damage within 10-15 mins

Stage 2 Inflammation – within 2-3 hrs of injury and may last up to 5 days – result of enzymes released and characterised by –
Calor (heat)
Rubor (redness) – local blood vessels forming an ↑ vascular bed
Tumor (swelling) – comprised of inflam exudate + blood
Dolor (pain) – due to chemicals released by damaged and dying cells acting on nerve endings AND an ↑ in local tis pres
All components cause loss of function

Tx RICE – Rest, Ice, Compression, Elevation
↓ bleeing – elevation (↓ pres in local vessels) + ice (vasoconstriction)
↓ pain – elevation (dispersed fluid via lymphatics thereby ↓ tis pres) + ice (neuromodulatory effect)
↓ swelling – ice + compression (↑ tis pres releasing exudates) + elev + gentle mus contraction (↑ lymphatics + ↑ VR)
Prevent further damage – relative rest (avoid complete rest) + prevent faulty mvment (eg limping can cause 2ndry damage)
Aid phagocytosis gentle mvment + US

Avoid HARM in inflammatory phase
Heat
Alcohol - ↑ bleeding through vasodilation
Rubbing (massage) - ↑ bleeding and disruption of clot formation
Movement (excessive) - ↑ inflam component

Stage 3 – Repair
Starts within 12 hours
Within 2-3 days – fairly extensive sys of new blood vessels therefore aiding repair via phagocytosis, ↑ protein and O2 diffusion
Cells multiply and lay down collagen fibers
Arrangement of scar fibers influenced by applied stress and responds to progressive loading
Tx Stimulate stress patterns via -
Joint and soft tis mobilisation
Passive stretching
Massage
Graded active mvment ensuring correct mvment patterns
Physiotherapy txs need to be applied in a progressive manner dependent on length of time into repair phase + pt response
Rehab –
Needs to be progressive and take into consideration – strength, flexibility, balance
Scar tis remodels over 6 months – continue w rehab over this time
Establish if any us imbalances exist if recurrent or multiple injuries

SUMMARY - ORTHOPAEDICS

Back Pain

1. Red Flags
a. Pt <20 or >50
b. Significant trauma
c. Systemic sxs – weight loss, fever, night sweats, lethargy
d. Neurological sxs – weak legs
e. Pain
i. Progressive
ii. Continuous
iii. Severe unremitting night pain
iv. Worse when recumbent
f. P.Hx
i. Ca
ii. IV drug use
iii. Systemic steroids
g. Exmn
i. Localised bony tenderness
ii. Pain over thoracic spine
2. Red Flags as per ACC guidelines
a. Trauma – in the older pt
b. Infection or Trauma
i. Age <20, >50
ii. Hx of ca
iii. Constitutional sxs – night sweats, fevers, weight loss, lethargy
iv. Infection RFs – incl occupation
c. Sxs of cord embaressment
i. Saddle anaesthesia
ii. Recent onset bladder dysfunction
iii. Progressive neurological deficit in leg(s)
3. Yellow Flags (psychosocial factors predictive of successful rehab)
a. Attitudes and beliefs about back pain
b. Behaviours
c. Compensation issues
d. Dx and Tx issues
e. Emotions – eg fear avoidance
f. Family
g. Work
4. Differentials – CPING
a. Congenital – scoliosis
b. Physical – trauma, strains, sprains, #, pathological #
c. Infection – discitis, osteomyelitis, TB
d. Inflammation – AS, RA, OA
e. Neoplastic – mets, primaries rare
f. Global – osteoporosis (pathological #s), osteomalacia, hyperparathyroidism
5. Management of a sore back when Ø red flags and Ø neuro sxs
a. 0-4 weeks duration
i. Self limiting
ii. Ø bed rest
iii. Education – safe lifting techniques, keeping active
iv. Exercises – esp swimming
v. Light duties at work
vi. Paracetamol, NSAIDs
vii. Manipulation, Physio, Acupuncture
b. 4-6 weeks duration → Reassessment – if Ø red flags or neuro sxs -
i. As per above but add ESR and X-ray
c. 6+ weeks duration
i. Refer for rehab and pain control
ii. Consider amitriptyline
6. Cauda Equina Syndrome
a. Definition – compression of cauda equine within lumbar spine → damage to sacral n roots
b. Etiology – sudden massive disc herniation
c. Presentation
i. Saddle anaesthesia
ii. Recent onset bladder dysfunction (sphincter dysfunction) – urinary retention
iii. Severe progressive neurological deficit (flaccid paralysis)
7. Sciatica
a. Defintion – pain radiating down lower limb along path of sciatic nerve + either of its two divisions
b. Etiology
i. Younger pt → disc prolapse
ii. Older pt → compression of n root by osteophytes
c. Presentation
i. Sharp pain
ii. Sensory sxs – tingling, numbness, dysaesthesia
iii. +/- Motor sxs
iv. +/- Reflexes ∆s
v. +/- Low back pain (usu less signicant than leg pain)
8. Degenerative Lumbar Disease
a. Aging
b. Disc nucleus desiccates + annular fissure develops → bulging disc → ↑ facet load
c. Complications
i. ↑ facet load → OA
ii. Bulging disc → narrowed root canal → n root compression → sciatica or neurogenic claudication
iii. Disc prolapse
9. Disc Prolapse
a. Localised annular fissure → bulging → failure of disc → nucleus prolapse → compression → sciatic or neurological disturbance
b. L5 and S1 nerve roots most common
i. L4/5 → L5 n root → ↓ power EHL, ↓ sens L5 dermatome, normal reflexes
ii. L5/S1 → S1 n root → plantarflex weakness, ↓ sens S1 dermatome, ↓ ankle reflex
c. Central and massive disc prolapse → cauda equina syndrome
d. Clinical features
i. Pt typically aged 20-50 + active (in elderly people, no longer capable of prolapse)
ii. Usu traumatic incident (can be minor)
iii. Lassague’s sign +ve → if SLR on supine pt is painful in buttock/back/other leg and restricted to <45 degrees
e. Management
i. Self resolving 1-6 weeks
ii. Excl cauda equina syndrome
iii. Acute stage - bed rest firm mattress, analgesia, epidural corticosteroid inj only if severe
iv. Surgery – only considered for severe dis or ↑ neurological impairment – eg foot drop or bladder sxs

Ankle Sprains

1. Definition
a. Soft tissue injury to supporting structures of joint – usu ligaments
2. Anatomy
a. Medial deltoid ligament → anterior and posterior tibio-talar, tibio-navicular, tibio-calcaneal
b. Lateral collateral ligament → 3 separates bands, more distinct, less robust
i. Anterior talo-fibular ligament (horizontal)
ii. Calcaneo-fibular ligament (vertical)
iii. Posterior talo-fibular ligament (horizontal)
3. Ankle Sprains
a. Almost always involve the lateral ligamentous structures
b. Anterior taol-fibular ligament – most vulnerable in plantarflexion + inversion (most common position for ankle sprains)
4. Classification of lateral ankle sprains
a. Grade 1 – mild stretching of ligament fibers, no laxity
b. Grade 2 – partial tear ant talo-fibular and calcano-fibular ligaments, good overall stability
c. Grade 3 – complete rupture ATF and CF ligs causing potentially unstable joint (↑ swelling but often ↓ pain due to n damage)
5. Clinical examination
a. Palpation over lateral ligamentous complex should elicit specific tenderness at site of ligament(s) involved
b. As injury becomes less acute, test for ligament instability
i. Talar tilt test – calcano-fib lig
ii. Ant drawer test – ant talo-fib lig
6. Ixs
a. XR – if suspected # or takes longer to settle than expected
b. Ottawa Ankle Rules (see picture)
i. 100% sensitive, 50-60% specific
ii. If there is no tenderness A→D and the patient can weight bear (4 steps regardless of limping) – it is NOT a #
7. Acute management lateral sprains
a. RICE
b. Crutches
c. Bandage or sleeve support (comfort)
d. Cast or splint – reqd for more severe/swollen sprains
e. Rehab once acute sxs begin to resolve → peroneal strengthening, range of motion exercises, proprioceptive training (eyes closed, balance on one foot)
f. Delay return to sport until rehab well on the way
8. Chronic lateral instability
a. Surgery indications – crippling instability preventing adequate level of function after adequate rehab attempted
b. Requires – 3x months supervised proprioceptive training + perineal strengthening and stress x-rays confirming degree of instability

Ankle Fractures

1. Hx
a. Sig event – unable to weight bear after event
b. Rapid onset of swelling (due to ankle haemarthrosis)
2. Exmn
a. Gross deformity
b. Ankle instability
c. Crepitus
d. Localised bony tenderness (ankle Ottawa rules)
i. Tenderness over medial ligaments has impt implications on ankle biomechanics and congruency
ii. Disruption over medial ligaments → significantly diminished contact area
iii. Displaced lateral malleolar #s do NOT result in altered joint contact area provided medial structures are intact
3. Ix
a. XR (AP, lat, mortoise +/- longer film if suspect # at head of fibula) – determine if ankle joint is congruently or incongruently reduced → incongruency requires surgical intervention (provided pts gen condition and soft tis allows)
4. Management
a. Ideal method of early stabilisation = padded plaster of paris back slab
b. Simple (closed) # + joint well reduced + Ø medial lig injury
i. Conservative tx w cast
ii. Weight bearing at 2 wks
iii. Crutches for 6 wks
c. Displaced # or if joint surface has been incongruent at some point
i. Internal fixation of # (fraught in elderly, conservative approach may be more appropriate)
ii. Surgical intervention if suspected disruption of medial ligaments
d. Open (compound) #
i. Early cultures to identify potential pathogens
ii. Initiate A/B cover (usu cephalosporin)
iii. Immediate (<6 hrs) debridement of contaminated tis + thorough irrigation of open injury
1. Debridement = excision of devitalised tis + foreign material from a wound
iv. An open joint must be closed otherwise leave all wounds open and revisit for closure at 48 hrs

Shoulder Injuries

1. Instability
a. Traumatic anterior dislocation
i. Etiology
1. Forced abduction + external rotation
2. Direct blow proximal humerus head pushing it forward + down
ii. Presentation
1. Severe pain
2. Inability to move shoulder
3. Obvious deformity
iii. Ixs
1. XR
2. Assess axillary nerve function – deltoid sensation, abduction
iv. Tx
1. Reduction – often requires sedation, analgesia and muscle relaxation (usu GA)
v. Mgt
1. High incidence recurrence
2. Surgical reconstruction (young + active)
3. Rehab
b. Anterior subluxation
i. Def → Passage of humeral head anteriorly out of joint + spontaneous reduction
ii. Ixs → look for evidence of minor #s glenoid rim
iii. Mgt → Rehab (mus strength + balance)
2. Rotator Cuff problems
a. Impingement / Tendonosus
i. Hx
1. Specific or repetitive shoulder injury
2. Pain/weakness with overhead activities
3. Night pain
ii. Exmn
1. Painful arc (70’-100’ abduction)
2. Tender over greater tuberositiy +/- biceps tendon
3. Weakness
4. Positive impingement sign
iii. Ixs
1. XR
2. US – assess cuff integrity
iv. Mgt
1. NSAID / Analgesic
2. Muscle strength and balancing program
3. Subacromial corticosteroid injection
4. Arthroscopic acromioplasty
b. Rotator cuff tear
i. Usu supraspinatus
ii. Hx
1. Specific injury normal
2. Similar pain to impingement but ↑ weakness
3. Stiffness / Frosen shoulder
iii. Exmn
1. ↓ active abduction arm but passive abduction ok
2. Weak RC muscles
iv. Ixs
1. US → reliably shows any sig RC tear
v. Mgt
1. Sig tears + weakness → surgical tendon repinsertion
2. Small tears + good function → rehab once pain settles
3. AC Joint injury
a. Etiology – falls, contact activities (impact on point of shoulder → pushes acromion + scapula away from clavicle)
b. XR – confirms joint separation, excl outer clavicle #s
c. Mgt – majority managed conservatively w sx relief (analgesia, icing, anti-inflam, sling)

Knee Ligament and Meniscal Injuries

1. Clinical features
a. Pop or snap → ACL injury
b. Pain – does not correlate w severity of injury
c. Swelling – impt indication of injury severity
i. Haemarthrosis → <1 hr onset, v painful → torn ACL until proven otherwise (2nd most likely cause = patellar disloc)
ii. Effusion → delayed swelling, normal looking synovial fluid, uncomfortable → minor sprain or meniscus
2. ACL
a. Most common knee ligament injury in sport
b. Non-contact wrenching injury
c. Feats – hear pop or snap, pain (unable to continue), haemarthrosis
3. PCL → less common – typically dashboard injury
4. Chronic ligament instability → muscle rehab and knee brace, or ligament reconstruction
5. Meniscal problems
a. Meniscal pathologies
i. Congenital
1. discoid (Øsemi-lunar) menisci (often asx but suscep to tearing)
2. hypermobile meniscus (cataching/locking)
ii. Acqd
1. younger – ligament injuries + subseq hypermobility
2. older – degenerative meniscal tears
b. Hx
i. Tender over joint line
ii. Pain and catching (on rotational mvments rather than straight line)
iii. Locking (then unlocking) – only occurs if sig meniscal fragment displaced in joint (inability to straighten leg)
c. Exmn
i. Effusion (often with meninscal tear)
ii. Localised tenderness over affected meniscus
iii. Meniscal grinding test → pain
iv. Excl assoc ligament injury (test all ligs) and patellar instability
d. Ixs
i. Clinical dx use, use MRI if unclear
ii. XR – to excl other conditions + assess degree of pre-existing degeneration of joint)
iii. Tear in avascular zone (central 2/3) – unlikely to heal
e. Tx
i. Arthroscopic tx (surgery through small stab incisions)
ii. Degenerative tears – resect unstable fragment
iii. Longitudinal tears – sutures or absorbable arrows
iv. Discoid menisci – resect abnormal portion, leave as much rim as possible
v. Symptomatic hypermobile menisci – suture menisci to capsule
f. Complications
i. Damage → predisposition to joint degeneration (wear and tear on remaining articular surface)

Soft Tissue Problems of the Lower Extremities

1. Tendon rupture – eg Achilles Tendon
a. Sxs
i. c/o of being kicked in the calf
b. Signs
i. Calf squeeze test (Thompson)
ii. Palpable defect
iii. Thickening, swelling, bruising
c. Tx
i. Aim – restore physical length
ii. Conservative – equinus cast
iii. Surgical – repair +/- augmentation
2. Peristalgia (most commonly used to refer to shin splitnts)
a. Def – o/load condition of the muscle insertions into the bone
b. Pres – diffuse pain along medial tibial border, usu middle/distal 1/3, disappears on warming but returns on cooling down after exercise
c. Tx – massage, correction of underlying biomechanical/postural abnormalities, ↓ training load to allow adaptation, graduated reintro of exercises, surgery rarely reqd
3. Stress # (shin splints)
a. Defintion
i. End stage of bone o/load
ii. Excessive load → abnormal physiological response in bone → bone reabsorption > production → focal weakness → stress # propogation
b. Anterior cortex under tension + poorer blood supply than posterior cortex
i. Slower healing
ii. ↑ risk of delayed or non-union
c. Exmn – focal tenderness, pain on hopping
d. Ixs – XR often normal, bone scan will confirm dx
e. Tx
i. Relative rest (may involve immobilisation, non-weight bearing)
ii. Education
iii. Graduated return to activity once pain free
iv. Surgery occasionally – plate, rod, debridement, bone graft
4. Principles of acute soft tissue injury management
a. Stage 1 – cellular damage 10-15 mins
b. Stage 2 – inflammation (within 2-3 hrs lasting up to 5 days)
i. Features
1. Calor – heat
2. Rubor – redness (↑ vascularity)
3. Tumor – swelling (inflammatory exudates + blood)
4. Dolor – pain (chemicals acting on n endings + ↑ local tis pres)
ii. RICE – rest, ice, compression, elevation
1. ↓ bleeding – elevation (↓ local pres) + ice (vasoconstriction)
2. ↓ swelling
3. ↓ pain – elevation (↓ tis pres)
4. Rest prevents further damage
iii. Avoid HARM – heat, alcohol, rubbing, movement (↑ inflammation)
c. Stage 3 – repair (Rehab phase)

Musculoskeletal Radiology

1. Terminology
a. Open (compound) or closed
b. Complete or incomplete
c. Location
i. Shaft – divide into 1/3s
ii. End of bones – anatomical description eg supracondylar #
d. Type
e. Displacement (ends of bones have shifted relative to one another)
i. Relative position of distal fragment compared to proximal fragment – lat/med or ant/post
ii. % terms (relative to width of bone), if displ >100% then describe length of overlap or amount of distraction
f. Angulation
i. Varus – distal fragment points medially
ii. Valgus – distal fragment points laterally
g. Rotation
i. Degrees – laterally or medially
h. Communition – 2 or more fragments (mild, mod, severe)
2. Incomplete # (line of # does not completely traverse bone) – usu children
a. Buckle # - focal compression cortex
b. Torus # - circumferential type of buckle
c. Greenstick # - periosteum + cortex fractured on one side, buckled on the other
d. Plastic bowing deformity – bending w/o discrete # line
3. Biomechanical loading on long bones
a. Tension or traction – pulling apart of trabeculae
b. Compression – pressing together of trabeculae
c. Torsion or rotation
d. Bending
4. # Configuration
a. Transvere – bending (eg direct blow)
b. Oblique – compression + torsion
c. Spiral – torsion or twisting
5. Growth plates injuries – Salter Harris system
a. Type 1 – SUFE
b. Type 2 – most common
c. In children – more likely that growth plate will # as opposed to ligaments being sprained → never dx a sprained lig in a child!
d. Complications → growth arrest, avascular necrosis
6. SUFE (slipped upper femoral (capital) epiphysis) – see picture
a. Growth plates slips into ER (adduction + extension)
b. Signs - ↓ IR, ↓ abduction, ↓ flexion
c. Common in heavy children – esp Polynesian boys 10-14 yrs age
d. Tx – screw across growth plate (goal is to keep plate from slipping, consider bilateral)
7. Pathological # - usu osteoporosis or tumor
8. Stress #
a. Fatigue # - abnormal stress, repetitive weakening of bone
b. Insufficiency # - 2ndry to normal stress on abnormal bone (es osteoporotis)

Biology of Pain
?Long answer question

1. Definition
a. Unpleasant sensory and emoal experience assoc w actual or potential tis damage
b. Pain perception – Ø correlation w degree of tis damage
c. Subjective
2. Classification – 2 main types of pain
a. Nociceptive – due to direct stim of peripheral n endings – eg burns, angina
b. Neuropathic – due to dysfunction in pain perception system within PNS or CNS, due to injury, dis or surgical damage
3. Alternative classification
a. Physiological
i. Nociceptive
ii. Non-nociceptive – predom due to SNS pain
1. Pathophys w or w/o afferent input to the sp cord/brainstem (eg chronic pain syndrome)
iii. Mixed nociceptive and non-nociceptive
b. Psychological
i. Somatoform d/os – somatisation d/o, conversion d/o, hypochondriasis – genuine but no physiological basis
ii. Factitious d/o – eg 2ndry intent
iii. Malingering
c. Mixed physiological and psychological
4. Pain physiology
a. A and C fibers – transmit from nociceptors to dorsal horn
b. Dorsal horn of spinal cord – 2nd order neuron spinothalamic tract subject to modulation additional to synapse w nocicepter fibers
i. Mechanoreceptors also synapse at dorsal horn
ii. Nociceptor neurons release NTs (eg subst P) in addition to excitatory transmitters → influence excitability of spinothal neurons
iii. Modulation by descending fibers from peri-aqueductal grey matter (midbrain) + raphe nuclei (medulla)
c. Dorsal horn is thus more than a waystation → it gates and modulates info about painful stimuli before sending it to the spinothalamic tract (integration + transmission)
d. Perception of pain further influenced in diencephalons by interconnections of thalamus to limbic system
e. Hypersens – LT potentialation via repeated depol of glycine/glutamate NMDA channels due to wind up
5. Components of pain → influencing pain perception
a. Biological factors
b. Social factors – eg job loss, role in family, friends, independence
c. Psychological factors – eg fear, anger, depression
6. Pain management
a. Mild → 1 g paracetamol
b. Moderate → add 30 mg codeine or 400 mg ibuprofen
c. Severe → add both 30 mg codeine and 400 mg ibuprofen
7. WHO analgesic ladder
a. Start → Non-opioid analgesic eg paracetamol, NSAID
b. Add → weak opioid eg codeine, dihydrocodeine
c. Substitute → replace weak opioid w strong opioid eg morphine
8. Opioid side effects
a. Constipation → regular laxative
b. Dry mouth → freq sips water, sugar free gum
c. N/V → anti-emetic
d. Sedation → explanation, avoid other sedating meds
9. Neuropathic pain
a. Features
i. Burning, stabbing, pulsing
ii. Spontaneous (w/o ongoing tis damage)
iii. Pain in area of sensory loss
iv. Presence of major neurological deficit (eg spinal cord trauma)
v. Pain in response to non-painful stimuli (allodynia)
vi. Hyperalgesia (↑ response to painful stimuli)
vii. Unpleasant abnormal sensations (dysaesthesias)
viii. Poor relief w opioids alone
b. Management
i. Antidepressants → amitriptyline
ii. Anticonvulsants → gabapentin
iii. Ketamine
10. Clinical Approach
a. Nociceptive element
b. Non-nociceptive physiological element → PHx or FHx pain, neuroendocrine (DM, thyroid), comorbids (eg migraine), neuro signs
c. Psychological element → PHx of FHx mental health probs, devtal hx
d. Consequential probs → impaired sleep, chr fatigue, depr, disuse atrophy
11. Mgt of chr non-ca pain → HOLISTIC (psych, social, pharm)
a. Psychological – CBT, exercise based mobilisation, mgt illness beliefs, tx of depr and others psyc conditions
b. Physiological – sleep restoration, analgesia, antidepressants, anticonvulsants, acupuncture, fitness
c. Vocational (ergonomic) and psychosocial – return to meaningful social engagement

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